BACKGROUND Formation of the Posterior Lateral Line system in zebrafish is pioneered by the posterior Lateral Line (pLL) primordium, a group of about 150 cells that forms near the ear. While leading cells in the pLL primordium have a relatively mesenchymal morphology, trailing cells are more epithelial; they have distinct apical basal polarity and they reorganize to sequentially form nascent neuromasts or protoneuromasts. The pLL primordium begins migration toward the tip of the tail at about 22 hours post fertilization (hpf). Proliferation adds to the growth of the primordium, nevertheless, as the primordium migrates, the length of the column of cells undergoing collective migration progressively shrinks as cells stop migrating are deposited from the trailing end: cells that were incorporated into protoneuromasts are deposited as neuromasts, while cells that were not, are deposited between neuromasts as interneuromast cells. Eventually, the primordium ends its migration a day later after depositing 5-6 neuromasts and by resolving into 2-3 terminal neuromasts. Establishment of polarized Wnt and FGF signaling systems coordinates morphogenesis and migration of the primordium: Wnt signaling dominates at the leading end and is thought to determine the relatively mesenchymal morphology of leading cells, while FGF signaling dominates in the trailing end. There, FGF determines reorganization of groups of trailing cells to form rosettes as they constrict at their apical ends. Furthermore, FGF signaling determines the specification of a central cell in each rosette as a sensory hair cell progenitor and it helps determine collective migration of the pLL primordium cells. Wnt signaling promotes its own activity and at the same time drives expression of fgf3 and fgf10. However, leading cells do not respond to these FGF ligands because Wnt signaling simultaneously promotes expression of intracellular inhibitors of the FGF receptor. Instead, the FGFs activate FGF receptors and initiate FGF signaling at the trailing end of the primordium, where Wnt signaling is weakest. There, FGF signaling determines expression of the diffusible Wnt antagonist Dkk1b, which counteracts Wnt signaling to help establish stable FGF responsive centers. Once established, the trailing FGF signaling system coordinates morphogenesis of nascent neuromasts by simultaneously promoting the reorganization of cells into epithelial rosettes and by initiating expression of factors that help specify a sensory hair cell progenitor at the center of each forming neuromast. Over time, the leading domain with active Wnt signaling shrinks closer to the leading edge and additional FGF signaling centers form sequentially in its wake, each associated with formation of additional protoneuromasts. QUESTIONS The interactions between the leading Wnt system and the trailing FGF system provide a useful framework for understanding the self-organization of neuromast formation and deposition by the migrating pLL primordium, however, many questions remain unanswered. The Wnt and FGF signaling systems act simply as a means of communication between cells and it remains unclear what molecular mechanisms are being regulated by them to specifically determine morphogenesis of epithelial rosettes and the collective migration of primordium cells. Furthermore, the mechanics of collective migration in the primordium remains poorly understood, specifically, how the pull of leading cells, which migrate in response to chemokine cues in their path, determines the FGF-dependent collective migration of trailing cells in the primordium. Finally, the summary above suggests that morphogenesis of epithelial rosettes during the assembly of nascent neuromasts is entirely dependent on FGF signaling. However, it has been seen that in the absence of collective migration mediated by chemokines in the leading cells, the trailing cells in the primordium come together to form one or two large rosettes. These and other observations related to the changes in the number and size of epithelial rosettes in the presence and absence of collective migration suggest that primordium cells have an inherent potential to form epithelial rosettes and their potential to form epithelial rosettes can be influenced by a variety of signaling systems and/or by migratory behavior of leading cells. Our attention has now shifted to answering some of the questions outlined here. Below we summarize the observations of a recently published study that describes the role of chemokine signaling in determining expression of the transcription factor Snail1b in leading cells, the role of Snail1b in kickstarting collective migration of the pLL primordium, and the surprising role of collective migration in determining sequential formation of protoneuromasts in the migrating primordium. CXCL12a INDUCES SNAIL1B EXPRESSION TO INITIATE COLLECTIVE MIGRATION AND SEQUENTIAL FGF-DEPENDENT NEUROMAST FORMATION IN THE ZEBRAFISH POSTERIOR LATERAL LINE PRIMORDIUM Our discovery that snail1b is expressed in leading cells led us to speculate that its expression might be determined by Wnt signaling and that, as a factor known for its role in promoting EMT, it might determine mesenchymal morphology of leading cells. However, our analysis revealed that Wnt signaling does not determine snail1b expression in the leading zone. Instead, its expression in the leading zone is promoted by chemokine signals first encountered by leading cells of the primordium, while Fgf signaling prevents snail1b expression in trailing cells. The effect of knocking down snail1b function was also not what we expected. It did not compromise the ability of leading cells to adopt a mesenchymal morphology. Instead, sequential morphogenesis of epithelial rosettes associated with formation of protoneuromasts in the trailing domain was delayed in snail1b morphants. Our analysis revealed, however, that the delay in protoneuromast formation is not related to a specific role of Snail1b in morphogenesis of epithelial rosettes. Instead, it is indirectly related to the role of Snail1b in helping to initiate effective collective migration of the primordium, a role consistent with its previously described role in promoting cell movement. Interestingly, we found that other manipulations that prevent effective primordium migration also cause a similar delay in sequential formation of Fgf signaling centers, associated protoneuromasts and shrinking of the leading Wnt system. These observations, together, reveal an unexpected role for collective migration of the primordium in kick-starting sequential formation of additional protoneuromasts. Finally, we showed that problems in initiating collective migration in the primordium may, at least in part, be related to aberrant expansion of the cell adhesion molecule epcam into the leading zone and/or the loss of cdh2 expression from the leading zone of the primordium following knock-down of snail1b function.